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Mecp2 is a DNA methylation reader that plays a critical role in experience-dependent plasticity. Increasing evidence supports a role for epigenetic modifications in activity-induced gene expression. Hence, candidate genes related to such phenomena are of great interest. Ryanodine receptors are intracellular calcium channels that contribute to hippocampal synaptic plasticity, dendritic spine remodeling, and participate in learning and memory processes. Here we exposed mice to the enriched environment (EE) paradigm, which through increased stimulation induces experience dependent-plasticity, to explore a role for methyl-cytosines, and Mecp2 in directing Ryanodine receptor 3 ( Ryr3 ) transcriptional activity. EE induced a hippocampal-specific increase in the methylation of discrete cytosines located at a  Ryr3  isoform promoter; chromatin immunoprecipitation experiments revealed that EE increased Mecp2 binding to this  Ryr3  isoform promoter. Interestingly, the experimental paradigm induced robust  Ryr3  upregulation, accompanied by  miR132 -dependent suppression of  p250GAP , a pathway driving synaptogenesis. In contrast to WT mice,  Mecp2-null  mice showed diminished levels of  Ryr3  and displayed impaired EE-induced  Ryr3  upregulation, compromising  miR132  dependent suppression of  p250GAP  and experience-dependent structural plasticity. Based on these results, we propose that Mecp2 acts as a transcriptional activator of  Ryr3 , contributing to experience-dependent plasticity.

Mecp2 Mediates Experience-Dependent Transcriptional Upregulation of Ryanodine Receptor Type-3